A Prominent Serine-rich Region in Vmw175, the Major Transcriptional Regulator Protein of Herpes Simplex Virus Type 1, is not Essential for Virus Growth in Tissue Culture

Paterson, Trevor; Everett, Roger D.

doi:10.1099/0022-1317-71-8-1775

Cited by 88 publications

(46 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For these studies we used a replication-defective HSV-1 expression vector, Cgal⌬3, that encodes lacZ. 17,18 This allowed us to monitor for infection and expression of the lacZ transgene by examining infected cells for their expression of ␤-galactosidase (␤-gal) by flow cytometry.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Chronic lymphocytic leukemia B cells are highly sensitive to infection by herpes simplex virus-1 via herpesvirus-entry-mediator A

Eling

Johnson²,

Sharma

et al. 2000

Gene Ther

View full text Add to dashboard Cite

We found that chronic lymphocytic leukemic (CLL) B cells are highly sensitive to infection with vectors derived from replication-defective herpes simplex virus-1 (rdHSV-1). CLL B cells were found to express high levels of herpes virus entry mediator (Hve) A, but not HveC, the other known receptor for HSV-1. An HveA cDNA from CLL cells was found to encode Arg→Lys and Val→Iso substitutions at amino acids 17 and 241, respectively. Nevertheless, this cDNA encoded a functional receptor for HSV-1 when transfected into Chinese hamster ovarian (CHO) cells. Antibodies to HveA could block rdHSV-1 infection of CLL cells and HveA-transfected CHO cells with similar efficiencies in vitro.

show abstract

Section: Introductionmentioning

confidence: 99%

“…18,31 It contains the Escherichia coli lacZ gene under the control of the human cytomegalovirus (CMV) promoter/enhancer within the short unique portion of the HSV-1 genome. Cgal⌬3 was propagated and assessed for its relative concentration of plaque-forming units (p.f.u.)…”

mentioning

confidence: 99%

Chronic lymphocytic leukemia B cells are highly sensitive to infection by herpes simplex virus-1 via herpesvirus-entry-mediator A

Eling

Johnson²,

Sharma

et al. 2000

Gene Ther

View full text Add to dashboard Cite

show abstract

“…[22][23][24] The application of multimutated HSV, rather than singlemutated HSV, can decrease it remarkably. Second, under the existence of HSV antibodies, a recombinant HSV-1 vector might not be able to deliver transgenes into glioma cells.…”

Section: ϫ6mentioning

confidence: 99%

Antitumoral effects of defective herpes simplex virus-mediated transfer of tissue inhibitor of metalloproteinases-2 gene in malignant glioma U87 in vitro: Consequences for anti-cancer gene therapy

et al. 2000

View full text Add to dashboard Cite

We set up experiments to evaluate the effects of defective herpes simplex virus (HSV)-mediated in vitro gene transfer of tissue inhibitor of metalloproteinases-2 (TIMP-2) in malignant glioma cells. Intrinsic TIMPs are known to be inhibitors of the strong invasive activities of matrix metalloproteinases in malignant gliomas. The defective HSV vectors dvSRaTIMP2 was engineered to express human TIMP-2 (hTIMP-2) with a combination of replication-competent HSV mutant, temperature-sensitive HSV-tsK, and amplicon plasmid-containing hTIMP-2. The hTIMP-2 gene was driven by the simian virus 40 promoter. The helper virus (HSV-tsK) was thermosensitive; consequently, this vector could proliferate only at 31.5°C. After infection of U87 human glioblastoma cells with the vector in vitro, expression of TIMP-2 was confirmed by reverse zymography. The U87 cells infected in vitro either with dvSRaTIMP2 or HSV-tsK were efficiently destroyed under replication-permissive conditions (at 31.5°C) and significantly lowered under replication-nonpermissive conditions (at 37°C). The invasive activity of U87 was clearly inhibited by dvSRaTIMP2 infection at both 31.5°C and 37°C. Our studies suggest that TIMP-2 expressing the defective HSV vector is possibly useful for the treatment of malignant brain tumors. Cancer Gene Therapy (2000) 7, 799 -805

show abstract

“…D30EBA is a strain 17-derived IE3 mutant deleted from codons 83-1236; it was obtained from Dr. Roger Everett (MRC Virology Unit, Institute of Virology, Glasgow, UK). 23 To package amplicon vectors, 3 ϫ 10 6 RR1 cells were plated in media containing 10% FCS; after 4 hours, the cells were transfected by adding 40 l of Lipofectin (Life Technologies), waiting 5 minutes, and then adding the amplicon DNA solution dropwise (30 g at 1 g/l in Dulbecco's modified Eagle's medium). After 6 hours, plates were fed with media containing 5% FCS.…”

Section: Hsv Vectorsmentioning

confidence: 99%

Efficient cotransduction of tumors by multiple herpes simplex vectors: Implications for tumor vaccine production

et al. 2000

View full text Add to dashboard Cite

Many gene therapy strategies would be enhanced by efficient transfer of multiple genes into the same cell. Herpes simplex viral amplicon (HSV) vectors are good vehicles for gene transfer because they accommodate large pieces of foreign DNA and transfer genes rapidly and efficiently. The current studies examine whether efficient cotransduction of tumor cells can be accomplished using multiple HSV vectors in a manner useful for clinical gene therapy. Interleukin-12 (IL-12) exists as a heterodimer, with components (m35 and m40) coded for by genes on two separate chromosomes. We constructed HSV vectors carrying either IL12m35 (HSVm35) or IL12m40 (HSVm40) or both genes (HSVm75) separated by an internal ribosome entry site to assess whether gene transfer using a single HSV vector constructed to carry multiple genes has any advantage over gene transfer using multiple vectors that are each carrying single genes. Because IL-12 and IL-2 have been found to have synergistic antitumoral activity, we further analyzed the biologic activity of tumor cells cotransduced by separate HSV vectors carrying genes coding for these two cytokines. The results demonstrate that multiple genes can be inserted into the same cell efficiently using multiple HSV vectors, and that these vectors allow rapid production of tumor vaccines expressing multiple cytokine genes. Thus, gene transfer using HSV may not be limited by the size of the DNA that each vector can accommodate. Immunizations with tumors cotransduced with HSVm35 and HSVm40 were equally effective in eliciting a cytolytic T-lymphocyte response and in protecting against tumor growth in vivo as immunization with tumors treated with HSVm75. Immunization with tumors cotransduced with HSVm75 and HSVil2 was superior to immunization with tumors transduced with either alone. The combination of IL-2-and IL-12-secreting tumor cells may be used as an effective immunization strategy against solid tumors. Cancer Gene Therapy (2000) 7, 581-588

show abstract

A Prominent Serine-rich Region in Vmw175, the Major Transcriptional Regulator Protein of Herpes Simplex Virus Type 1, is not Essential for Virus Growth in Tissue Culture

Cited by 88 publications

References 49 publications

Chronic lymphocytic leukemia B cells are highly sensitive to infection by herpes simplex virus-1 via herpesvirus-entry-mediator A

Chronic lymphocytic leukemia B cells are highly sensitive to infection by herpes simplex virus-1 via herpesvirus-entry-mediator A

Antitumoral effects of defective herpes simplex virus-mediated transfer of tissue inhibitor of metalloproteinases-2 gene in malignant glioma U87 in vitro: Consequences for anti-cancer gene therapy

Efficient cotransduction of tumors by multiple herpes simplex vectors: Implications for tumor vaccine production

Contact Info

Product

Resources

About